What molecular mechanisms underlie the modulation of Mosquitoes host detection by bacterial infections?
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Bacterial infections can modulate mosquito host detection through various molecular mechanisms. One mechanism involves the disruption of interkingdom communication between bacteria and mosquitoes, which affects mosquito attraction to hosts. For example, the quorum-sensing inhibitor furanone C-30 can reduce the attraction of Aedes aegypti mosquitoes to a blood meal by disrupting the communication between the skin-inhabiting bacterium Staphylococcus epidermidis and the mosquitoes . Another mechanism involves the activation or inhibition of immune signaling pathways in mosquitoes. The Toll pathway, a major immune signaling pathway, plays a role in the antifungal immune response in mosquitoes. Activation or inhibition of this pathway can affect the immune response and pathogenicity of fungi such as Beauveria bassiana in mosquitoes . Additionally, the transcriptional axis involving the aryl hydrocarbon receptor (AhR) and TIEG has been found to modulate immune response negatively in mosquitoes. Activation or inhibition of AhR can compromise or enhance the anti-bacterial immunity in mosquitoes, respectively . Furthermore, the mosquito gut can discriminate pathogens from other microflora through the induction of a damage signal. This signal, mediated by the dorsal switch protein 1 (Aa-DSP1), triggers a signaling pathway that leads to the production of reactive oxygen species and immune responses in the gut . Overall, these molecular mechanisms highlight the complex interactions between bacterial infections and mosquito host detection.
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